(known as EMT), the process of transformation from epithelial cells to matrix-producing fibroblasts, that may ultimately result in renal interstitial fibrosis and renal failure. EMT is regulated by numerous hormones and growth factors, including tumor growth factor beta1 (TGF-beta1). Youhua Liu and colleagues from the University of Pittsburgh School of Medicine demonstrate that expression of the intracellular enzyme integrin-linked kinase (ILK) is specifically induced in renal tubular epithelial cells in response to TGFbeta1 and that ILK administration induces many key events in TGFbeta1-induced EMT. The data implicate ILK as a crucial mediator of EMT in renal interstitial fibrosis. The authors demonstrate that administration of a kinase-dead form of ILK abolishes TGFbeta1-induced EMT suggesting that this and other inhibitors of ILK signaling could be explored as potential therapies for chronic renal disease.

TITLE: Role for integrin-linked kinase in mediating tubular epithelial to mesenchymal transition and renal interstitial fibrogenesis

AUTHOR CONTACT:
Youhua Liu
University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Phone: (412) 648-8263
Fax: (412) 648-1916
E-mail: liuy@msx.upmc.edu

View the PDF of this article at: https://www.the-jci.org/press/17913.pdf

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Interfering interferons in medulloblastoma

Type I interferons (IFN-alpha and IFN-beta), crucial for fighting viral infection and regulating immune function, signal via activation of STAT1 and STAT2. Iain Campbell and colleagues from the Scripps Institute in La Jolla, California, show that in mice lacking STAT2, IFN-alpha retains potent biological activity in the central nervous system. IFN-alpha mediates a type Ilike immune response with IFN-gamma gene expression and signaling in the brain associated wit
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Aug-2003

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